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M
A
T C
INTR
ODUCTION
T
oxic colitis and megacolon fall within the spectrum of inammatory bowel disease (IBD). Toxic colitis, also referred to as acute,
fulminant, or severe colitis, is a potentially life-threatening form
of IBD. Patients display gastrointestinal symptoms in conjunction
with signs of systemic toxicity. In its rare, extreme manifestation—
toxic megacolon—toxic colitis is accompanied by radiographic
evidence of nonobstructive colonic dilatation in excess of 6 cm.
Systemic toxicity distinguishes toxic megacolon from nontoxic
causes of colonic distention such as acute colonic pseudo-obstruction
(Ogilvie syndrome) or Hirschsprung disease. Even in the current
era of enhanced medical management and surgical technique, toxic
colitis and megacolon are associated with considerable morbidity
and mortality. Successful treatment of these patients requires the
close collaboration of surgeons and gastroenterologists. In this
chapter we review the latest thoughts on management of toxic colitis and megacolon.
EPIDEMIOLOGY AND
e incidence of toxic colitis and megacolon has decreased as the
options for medical treatment of IBD have expanded. Toxic colitis aects
approximately 10% of patients with ulcerative colitis (UC) and 6% of
those with Crohn colitis. e incidence of toxic megacolon is 1.6% to
13% in patients with UC and 2.3% for patients with Crohn disease. Both
toxic colitis and megacolon are more likely to aict patients early in
their disease course, sometimes as the initial presentation of the disease.
In the absence of a prior diagnosis of IBD, toxic colitis must be dierentiated from other conditions such as an infectious or ischemic colitis.
Patients with well-established IBD may also experience toxic colitis or
megacolon at any time during their disease. Toxic colitis and megacolon
show no anity for a particular age or gender.
Recently, infection has surpassed IBD as the most frequent cause
of toxic megacolon (Table 37-1). Although the most common infec-
tious source—Clostridium dicile–related pseudomembranous colitis—is associated with a 0.4% to 4.3% incidence of toxic megacolon, its
toxicity is due to the toxins produced by the bacteria themselves. is
mechanism is dierent from the toxicity of the inammatory process
in the bowel wall that is the feature of toxic UC or Crohn disease.
Among other infectious causes of toxic megacolon are bacterial infections such as Salmonella, Escherichia coli, and Campylobacter; viral
infections such as cytomegalovirus (CMV); and parasitic infections
such as cryptosporidium. Behçet disease, ischemic colitis, and colonic
lymphoma have also been associated with toxic megacolon. A review
of patients who underwent surgery for toxic megacolon from 1985 to
2004 determined that the underlying causes consisted of UC in 46%,
infectious colitis in 34%, ischemic colitis in 11%, chemotherapy in
3%, and Crohn disease in 2%. However, in the second half of the study
period, infections eclipsed UC as the origin of toxic megacolon (from
ETIOLOGY
M
Ursula M.
14% vs. 30% t
infections, in particular, is rising as a result of increased antibiotic use,
an aging population, and more virulent strains. Patients with human
immunodeciency virus and acquired immunodeciency syndrome
are particularly susceptible to toxic megacolon from C. dicile, as
well as CMV infections.
P
e pathophysiology of toxic colitis and megacolon has not yet been
well dened. A link between colonic inammation and diminished
smooth muscle contractility has been well established, and toxic
megacolon is more common in patients with pancolitis. Whereas
uncomplicated UC is characterized by inammation conned to the
mucosa and submucosa, UC-associated toxic megacolon is dened by
inammation that has spread into the muscularis propria. Moreover,
the severity of the colonic distension is directly related to the extent
of the transmural inammatory process. Apparently the myenteric
plexus has no role in the disease process, but enzyme-inducible nitric
oxide synthase, which produces the nonadrenergic, noncholinergic
neurotransmitter nitric oxide, has been shown to be more active in
patients with UC and, to a greater degree, with UC-associated toxic
megacolon. Synthesized by macrophages and smooth muscle cells,
nitric oxide promotes smooth muscle relaxation in the colon, an
eect that is magnied by its overproduction in the inamed bowel.
By inhibiting enzyme-inducible nitric oxide synthase in animal and
in vitro models, improvements were achieved in colonic distention
and pressure. In addition to nitric oxide, groups have studied hydrogen peroxide (H
to the genesis of toxic megacolon by promoting smooth muscle relaxation. Colonic motility may also be adversely impacted by inammation-induced changes in neuromuscular signaling.
PRESENTATION
P
atients with the acute onset of severe bloody diarrhea, abdominal pain, malaise, and anorexia should be suspected of having toxic
colitis, especially if IBD has previously been diagnosed. Toxic megacolon should be considered in a patient with symptoms of severe
colitis—particularly bloody diarrhea—in addition to increasing abdominal distention. e symptoms of severe colitis that are
refractory to treatment are usually present for 1 week before toxic
megacolon develops.
DIA
I
n a patient presumed to have toxic colitis and/or megacolon,
a thorough history should be obtained (Figs. 37-1 and 37-2).
Szmulowicz and Victor W. Fazio
o 39% vs. 14%, respectively). e incidence of C. dicile
ATHOPHYSIOLOGY
) a
nd interleukin (IL)-1β as potential contributors
2O2
GNOSIS
191
192
ManageMent of acute to
xic
colitis
and Megacolon
TABLE 37-1 Causes of Toxic Megacolon
Mechanism Examples
nammatory Behçet disease
I
Crohn colitis
Ulcerative colitis
Infectious Aspergillosis
Campylobacter
Clostridium dicile
Cryptosporidium
Cytomegalovirus
Entamoeba
Escherichia coli 0157
(hemolytic-uremic syndrome)
Rotavirus
Salmonella
Shigella
Yersinia
Ischemic colitis
Collagenous colitis
Volvulus
Cancer-related causes Chemotherapy
Colonic lymphoma
Kaposi sarcoma
Obstructive colorectal cancer
Stem cell transplantation
uestions should focus on the cause of the condition, differenti-
Q
ating between infectious and inflammatory conditions, especially
with de novo presentations. Inquiries are directed to a previous
diagnosis of IBD and a history of exacerbations, and extraintestinal manifestations such as arthritis, iritis, or liver disease also
should be sought. If IBD has not been previously diagnosed, then
pre-existing symptoms that could signal an undiagnosed IBD
are important: abdominal pain, diarrhea, bloody stools, vomiting, or weight loss. The possibility of exposure to a gastrointestinal pathogen via close contacts, the environment, or travel
should be explored. Current or recent use of medications—particularly antibiotics, anticholinergic agents, narcotics, or antidiarrheal agents—that could incite the episode of toxic colitis and/
or megacolon is documented. Other factors include a recent
barium enema or colonoscopy, hypokalemia, antiinflammatory
medications, antidepressants, CMV infection, or an overly rapid
or abrupt cessation of steroids, sulfasalazine, or 5-ASA medications. Also, ongoing use of certain medications such as opiates and
steroids could blunt the symptoms and signs of systemic toxicity
at the initial presentation. It is important to note if the patient
is immunocompromised as a result of human immunodeficiency
virus, malignancy, or chemotherapy.
EVALUATION
e severity of UC is gauged by criteria proposed by Truelove and
Th
Witts (Table 37-2). A patient who satisfies a greater number of
these criteria at the time of admission has a higher risk of urgent
colectomy—48% for three or more criteria. The clinical criteria
for toxic megacolon, as submitted by Jalan and colleagues, incorporate physical signs of toxicity with evidence of colonic dilatation (Table 37-3). Although a colonic diameter of 6 cm confirms
a diagnosis of toxic megacolon, a lesser degree of dilatation
does not arbitrarily exclude this diagnosis. Another sign of toxic
dilation is a gas pattern that shows distended transverse colon for
the entire length of the segment. Overall, though, it is the physician’s clinical impression that best distinguishes the patient with
toxic colitis or megacolon.
Signs of systemic toxicity are tachycardia, hypotension, and/or
postural hypotension, oen with a fever. Patients may display an
altered sensorium. Abdominal examination is usually characterized
by tenderness and reduced bowel sounds, whereas patients with toxic
megacolon have abdominal distension. Signs of peritoneal irritation
are consistent with a free perforation. However, the appearance of
some patients may belie the severity of their underlying condition,
usually as a result of medications such as narcotics or steroids. In this
situation, clinical acumen should be trusted.
e severity of the inammatory process may be reected by
elevations in the white blood cell count, C-reactive protein, and/or
erythrocyte sedimentation rate. A complete blood cell count and
electrolyte panel highlight nonspecic anemia and electrolyte abnormalities that should be aggressively corrected. Both hypokalemia and
hypoalbuminemia are common in patients with severe diarrhea. To
rule out an infectious cause—especially in patients without a prior
diagnosis of IBD—blood and stool cultures, as well as stool samples
for the C. dicile A and B toxins and for ova and parasites, should be
collected.
Imaging studies should be performed upon admission to detect
toxic megacolon and free perforation. Radiographic factors predictive of a colectomy in patients with toxic colitis include mucosal
islands—that is, normal mucosa amid deep ulcerations—and a colonic
diameter greater than 5.5 cm. e plain abdominal radiograph serves
as the primary modality for the initial determination of the presence and extent of colonic distention. Findings consistent with toxic
megacolon involve a colonic diameter greater than 6 cm; multiple
colonic air-uid levels; blunting or loss of colonic haustra; and small
bowel distention. Although the mean diameter of the dilated colon is
9.2 cm, it may range up to 15 cm. Colonic distention disproportionately
aects the ascending and transverse colon. Computerized tomography
(CT) has become a common method for the diagnosis of toxic colitis
and megacolon. e CT appearance of toxic colitis reveals pancolonic
wall thickening, submucosal edema, ascites, and pericolic fat stranding. In the acute setting, a thickened colonic wall does not dierentiate between UC and Crohn disease. In contrast, toxic megacolon can
be associated with segmental wall thickening, small bowel distension,
an abnormal haustral pattern, and pseudopolyps on a CT scan. e
diameter of the dilated colon is more eectively gauged by a CT scan
than by an abdominal radiograph. However, the value of a CT scan lies
in its ability to detect the complications of toxic colitis and megacolon, which might otherwise be overlooked clinically: intra-abdominal
abscess, ascending pyelophlebitis, and perforation. On ultrasound,
toxic megacolon exhibits attenuated walls, a diameter greater than 6
cm, intracolonic gas, and an absence of haustration.
e use of lower endoscopy in the assessment of toxic colitis and
megacolon is controversial. e severity of the colitis seen on endoscopy oen varies from that suggested by clinical symptoms and signs,
which may aect therapeutic decisions. Endoscopic ndings also may
have prognostic value, in that deep ulcerations to the muscularis propria—viewed as mucosal islands on plain abdominal radiographs—
frequently herald a failure of medical management. Yet a colonoscopy
is generally opposed in this acute setting, when the inamed, ulcerated colon is at very high risk of perforation. Moreover, a colonoscopy may precipitate toxic megacolon. However, a limited exible
sigmoidoscopy without a bowel preparation may aid in identifying
the underlying cause of the disease process, particularly in patients
without a prior diagnosis of IBD. A C. dicile infection is signaled by
the presence of pseudomembranes—that is, yellow-white supercial
plaques with interposed normal mucosa. Ischemic colitis is patchy,
with areas of preserved normal mucosa between ischemic ulcers, particularly in elderly patients. In addition, the rectum is rarely aected,
whereas in persons with UC, the rectum is always diseased. A colonic
Toxic
colitis
History and physical
Labs and stool studies
Abdominal radiograph ± CT scan
Consider flexible sigmoidoscopy
Free air, shock,
peritonitis, or
hemorrhage Clinically stable
COLON
193
Surgery
Clinical
deterioration
Transition to oral steroids + oral
6-mercaptopurine or
azathioprine versus infliximab
Clinically stable
orithm for the management of toxic colitis. CT, Computerized tomography; I V, intravenous.
FIGURE 37-1
iopsy may disclose inclusion bodies or trophozoites consistent with
b
Alg
Clinical deterioration
Clinically stable
Consider
cyclosporin or
infliximab
Improvement
Outpatient
management
CMV or fulminant amoebic colitis, respectively, although biopsies do
not reliably distinguish UC and Crohn disease during an acute episode. During endoscopy, minimal air insuation is used, the scope
is advanced with great care, and a biopsy is performed with caution.
MEDIC
ective management of the seriously ill patient with toxic colitis
E
AL MANAGEMENT
and megacolon relies on the participation of gastroenterologists, surgeons, intensivists, and radiologists. e goal of medical therapy is to
treat the precipitating disorder, medically stabilize the patient, and
prevent associated complications. e patient requires close monitoring with frequent assessment of vital signs and hydration status and
regular abdominal examination for early detection and treatment of
signs of clinical deterioration such as hypotension and tachycardia.
Worsening of abdominal tenderness and distension are also very
concerning. Although seemingly suggestive of an improvement in
toxicity, a decrease in the frequency of watery bowel movements or
of bowel sounds may instead indicate the onset of toxic megacolon.
Laboratory studies should be performed twice daily so that electrolyte abnormalities (especially hypokalemia and hyponatremia), along
Close monitoring
Supportive care
IV corticosteroids
Improvement
Transition to
oral steroids
Clinical
deterioration
Surgery
Clinical
deterioration
Clinically
stable
Outpatient
management
with dehydration and anemia, all of which exacerbate colonic atony,
can be aggressively corrected. Plain abdominal radiographs, including a le lateral decubitus or upright view, should be obtained once
or twice daily to identify and/or to follow the evolution of the colonic
distension and to exclude the presence of free air. Toxic megacolon
may appear suddenly even if the clinical status of the patient remains
otherwise unchanged. Among the signs of clinical improvement are
the normalization of the pulse, temperature, and white blood cell
count, as well as resolution of the colonic dilatation. Medications that
may have precipitated the onset of toxic megacolon—particularly
preadmission antibiotics, anticholinergic agents, and antidiarrheal
medications—should be withdrawn. Similarly, narcotics should be
used cautiously, also because of their masking eect on symptoms.
e patient may be as active as is tolerated, as long as no mental status changes occur. Maintenance of bowel rest is controversial because
it has not been shown to promote recovery in patients with toxic
colitis and megacolon. Similarly, intravenous (IV) nutrition has no
benet for hastening recovery or for preventing colectomy and risks
the development of complications from central venous catheters.
e need to provide adequate nutrition via the enteral or parenteral
route should be balanced with the clinical condition of the patient.
In the absence of emesis, a nasogastric tube is usually not warranted
because it does not relieve colonic distension. Instead, some groups
194
ManageMent of acute to
xic
colitis
and Megacolon
Toxic
megacolon
History and physical
Labs and stool studies
Abdominal radiograph ± CT scan
Consider flexible sigmoidoscopy
Free air, shock,
peritonitis, or
hemorrhage Clinically stable
Clinical deterioration or
Surgery
Outpatient
management
FIGURE 37-2
Computerized tomography; I V, intravenous.
T
ABLE 37-2
of Ulcerativ
Criterion
failure to improve
Clinically stable
Alg
orithm for the management of toxic megacolon. CT,
Clinical Criteria f
e Colitis
Mild
Disease
Se
vere
Disease
or the Severity
Close monitoring
Supportive care
IV corticosteroids
Improvement
Transition to
oral steroids
Clinical
deterioration
Surgery
Fulminant
Disease
Stools per day <4 >6 >10
Blood in stool Infrequent Frequent Continuous
Temperature,
Heart rate, beats
°
C No
rmal >37.5 >37.5
Normal >90 >90
per minute
Hemoglobin Normal <75% of
baseline
Erythrocyte
<30 >30 >30
Transfusion
required
sedimentation
rate, mm/hr
Abdominal
— Edema Dilatation <6 cm
radiograph
Clinical signs — Abdominal
tenderness
Abdominal
tenderness and
distention
odied from Truelove SC, Witts LJ. Cortisone in ulcerative colitis; nal
M
report on a therapeutic trial. BMJ. 1955;2:1041-1048.
TABLE 37-3 Clinical Criteria for Toxic Megacolon
Radiogra
colonic distention
M
Secondary criteria (at least
M
tive colitis: toxic dilation in 55 cases. Gastroenterology. 1969;57:68-82.
advocate redistributing intracolonic gas by frequent maneuvering of
the awake, cooperative patient with toxic megacolon via rolling or
by assuming the prone-knee-elbow position. Antithromboembolic
prophylaxis should be instituted.
advanced since the introduction of IV corticosteroids in the 1950s.
Generally, toxic colitis is treated similarly in patients with UC and
Crohn disease. In patients with an underlying IBD, the primary
agents are high-dose IV steroids—either hydrocortisone (100 mg
every 6 hours) or methylprednisolone (60 mg daily). e response
of toxic colitis to high-dose IV corticosteroids ranges from 47% to
75% within 5 to 7 days, although the eect persists for 3 months in
only 37%. Neither more potent steroids nor continuous steroid infusions have improved the results. Steroids should be started immediately upon the diagnosis of toxic colitis or megacolon and halted if an
infectious cause is later discovered. Once the acute episode resolves,
the patient is transitioned to oral prednisone, which is then tapered.
Among the ndings that strongly portend a colectomy are more than
three to eight stools per day and a C-reactive protein value greater
than 45 mg/L aer 3 days of steroid treatment, with an 85% risk. Studies have not reliably demonstrated an increased incidence of postoperative complications as a result of high-dose IV steroids. Of course,
steroids may mask the signs and symptoms of clinical deterioration.
toxic colitis. If the patient does not respond to corticosteroids alone
aer 2 to 4 days but is not clinically declining, cyclosporin (2 to 4
mg/kg IV per day) may be included as a fast-acting rescue agent to
avoid a colectomy. In the short term, 67% to 80% of patients who are
treated with this dual regimen avoid a colectomy; however, once the
cyclosporin is withdrawn, the long-term response rate falls to 42%
to 60%. Also, the medication has signicant adverse eects, including neurotoxicity, seizure, renal toxicity, hypertension, and opportunistic infection. However, cyclosporin has not been shown to aect
the complication rate of an urgent colectomy. For long-term maintenance therapy, a patient responsive to cyclosporin is ultimately
switched to oral 6-mercaptopurine or azathioprine, neither of which
is used in the acute management of toxic colitis; these immunosuppressive medications maintain the probability of averting a colectomy
over a longer interval. Like cyclosporin, the monoclonal anti–tumor
necrosis factor antibody iniximab (5 mg/kg for one dose) has been
demonstrated to avert short-term colectomy in up to 90% of patients.
However, use of this monoclonal antibody is associated with opportunistic infections, malignancy, and infusion reactions. Studies of the
eect of the monoclonal antibodies on the morbidity of colectomy
are inconclusive. Cyclosporin and iniximab are similarly ecacious
as second-line rescue agents, with colectomy rates of 17% and 21%,
respectively, in one randomized trial. Sequential use of the medications is not recommended. Cyclosporin and iniximab have not been
phic evidence of
ain criteria (at least three) Fever >38.5
achycardia >120/min
T
Leukocytosis >10.5 × 10
H
emoglobin <60% of baseline
°
C
9
/L
Altered mental status
one)
Dehydration
Electrolyte imbalances
Hypotension
odied from Jalan KN, Sircus W, Card WI, etal. An experience of ulcera-
Specic medical management of toxic colitis and megacolon has
New second-line agents have been added to the treatments for
COLON
195
vestigated in the treatment of toxic megacolon. Oral agents such as
in
sulfasalazine and 5-aminosalicylate have no role in either condition.
e use of prophylactic antibiotics in IBD-related toxic colitis and
toxic megacolon is controversial. Some groups favor broad-spectrum
antibiotics such as metronidazole and ciprooxacin because of the
possibility of bacterial translocation and an eventual perforation of
the weakened, ulcerated colonic wall. However, there is no dierence
in outcome when prophylactic antibiotics are included in the treatment regimen. Patients with toxic megacolon due to C. dicile coli-
tis require treatment with IV metronidazole (500 mg every 8 hours)
and/or vancomycin (500 mg orally or by nasogastric tube every 6
hours). Cytomegalovirus-associated toxic megacolon is treated with
IV ganciclovir (2.5 mg/kg every 8 hours or 5 mg/kg every 12 hours).
SURGIC
Indications f
e need for surgery must be evaluated repeatedly in patients with
toxic colitis and megacolon, and early surgical consultation is strongly
recommended. e surgeon must communicate with the patient and/
or the family about the possibility for a colectomy from the start of
the hospitalization. Among the absolute indications for immediate
surgery are free perforation, generalized peritonitis, uncontrolled
colonic hemorrhage, shock, and clinical deterioration despite optimal
medical management. Some patients will require emergency surgery
immediately upon presentation to the hospital. Less obvious is the
interval at which surgery should be performed if the patient does not
demonstrate clinical improvement. Most groups advocate surgery if
the patient has not improved aer 48 to 96 hours of aggressive medical treatment. In patients who have neither signicantly improved
nor worsened aer 5 to 7 days of therapy, surgery is also advisable.
Factors that signal a failure of medical management involve persistent signs and symptoms, such as diarrhea with or without hematochezia, abdominal tenderness, tachycardia, pyrexia, or a leukocytosis,
despite treatment; recurrent symptoms once the corticosteroids are
tapered; worsening symptoms regardless of medical therapy; and
the development of complications as a result of the medications. For
some groups, toxic megacolon on its own is an absolute indication
for immediate surgery because of the risk of perforation. However,
in other centers it is the persistence of colonic distention beyond 24
to 72 hours or its rapid progression as shown on plain abdominal
radiographs that prompts a colectomy. Failure of medical therapy
(44%) and toxic megacolon (42.2%) remain the primary reasons for
an urgent colectomy, in addition to hemorrhage (7.7%), perforation
(7.0%), and “other” (2.3%). Overall, toxic megacolon has become a
less common indication for surgery, with the incidence decreasing
from 71.1% in 1975-1984 to 21.6% in 1995-2005, likely as a result of
the enhanced medical treatment of colitis.
Approximately 20% to 40% of patients with toxic colitis will
require a colectomy, and the overall morbidity and mortality associated with surgery for toxic colitis and megacolon are decreased by
early intervention. By deferring surgery, the risk of complications
such as perforation or abdominal compartment syndrome, which
herald a poorer prognosis, increases. e mortality associated with
surgery for toxic megacolon varies from as high as 51% to as low as
2% to 8% with and without a perforation, respectively. In general, the
morbidity and mortality associated with surgery for toxic colitis and
megacolon have lessened in the past several decades.
AL MANAGEMENT
or Surgery
Surgical Options
everal procedures have been described for the surgical management
S
of toxic colitis and megacolon. e goal is to perform the safest procedure that will allow the patient to complete medical treatment and
recover his or her health. e selected operation may be the initial
stage of a multistage surgery.
Issues to consider are the underlying cause of the toxic colitis
and/or megacolon; the type and duration of the immunosuppressive treatment; the current medical status (“too sick for surgery”);
the comorbidities, including the status of the anal sphincter; and the
psychological tolerance of a permanent ileostomy. Informed consent—particularly focusing on the certainty of an end ileostomy and
the possibility of subsequent procedures—should be obtained from
the patient and/or family. Preoperative stoma marking is essential
to avoid later stoma complications, even if an additional procedure
is later anticipated. A bowel preparation is not required, but preoperative antibiotics and antithromboembolic measures are recommended. Intraoperatively, the condition of the colon will determine
the surgical strategy.
e surgical options for toxic colitis or megacolon are a subtotal
colectomy with ileostomy; a total proctocolectomy with an end ileostomy; and a loop ileostomy with a “blowhole” colostomy. For patients
with toxic colitis, an ileorectal anastomosis or ileoanal pouch procedure, with or without a temporary loop ileostomy, may be completed
at the time of the subtotal colectomy or total proctocolectomy, but
these procedures are extremely uncommon and are only performed
in very unusual circumstances because of the high degree of risk.
e most commonly performed procedure for toxic colitis and/or
megacolon is a subtotal colectomy with an end ileostomy. e technique removes the diseased colon while avoiding a risky anastomosis,
as well as a potentially morbid rectal dissection. It is the safest procedure, especially in the setting of a free perforation or toxic megacolon. A minimally invasive subtotal colectomy—either laparoscopic
or hand assisted—is also feasible and safe in selected patients with
otherwise uncomplicated toxic colitis, with a 3.4% to 6% conversion
rate, a 0.6% mortality rate, and a 16% to 37% complication rate. In
contrast, an open subtotal colectomy for toxic colitis carries an overall morbidity rate of 20% to 70%, including ileus and small bowel
obstruction, wound infection, intra-abdominal abscess, and rectal
stump dehiscence, and a 0% to 10% mortality rate. e procedure
is performed with the patient in the supine or low lithotomy position via a vertical midline incision. In patients with toxic megacolon,
the distended colon can be decompressed using a large-gauge needle
attached to suction. During the procedure, to facilitate a potential
subsequent ileoanal pouch reconstruction, the ileal branches of the
ileocolic vessels should be preserved and the terminal ileum should
be mobilized only to the extent that an end ileostomy is able to be
created. Moreover, to prevent adhesions that may later sabotage a
pouch procedure, dissection at the root of the mesentery and within
the pelvis is avoided and the sigmoid branches of the main trunk of
the inferior mesenteric vessels are divided close to the colonic wall.
e colon should be transected distally at the rectosigmoid junction,
leaving enough length for a tension-free attachment of the sigmoid
colon to the abdominal wall.
e oversewn distal end of the bowel is managed by one of several
t
echniques, based on the observation that the fragile bowel may not
hold sutures. It is ideally implanted without tension extrafascially in
the lower portion of the vertical midline wound, with its muscular
wall sutured to the surrounding fascia and the overlying skin closed.
Should a stump “blowout” occur, as is the case in 6.7% of patients,
the drainage will exude from the skin incision, which can then be
pouched. Alternatively, a rectal stump that is too inamed to allow
for staples or sutures may be completely exteriorized 5 to 8 cm above
the skin level and its open end wrapped in gauze to x it in place.
Aer 7 to 10 days, once the bowel becomes suciently fused to the
abdominal wall, the stump projecting beyond the skin is amputated
and the mucus stula is matured. Sometimes the rectal remnant can
be primarily matured into a mucus stula, or it can be oversewn and
le within the pelvis. However, a blowout of an intraperitoneal rectal
stump risks an abscess or sepsis. e rectal stump should be about 15 cm
in length to reduce the possibility of a suture line blowout. If the
rectum is too short to reach the abdominal wall, the distal sigmoid
196
ManageMent of acute to
xic
colitis
and Megacolon
ay be included in the Hartmann pouch. Extrafascial implantation
m
or mucus stula creation aid in the later identication of the rectal
stump. If none of these techniques is practicable because of perforation and/or marked friability of the bowel wall, then the proximal end
of the rectosigmoid can be le open within the peritoneum and surrounded by multiple drains; an additional drain is placed transanally
via the rectal stump. In patients for whom colonic hemorrhage is the
indication for surgery, the retained rectum infrequently remains a
source of signicant blood loss, which can be addressed via corticosteroid irrigation or, rarely, near-total proctectomy with preservation
of the anal sphincters and the distal anorectum (an ultra-low Hartmann pouch). Some groups advocate leaving a rectal tube to decompress the rectum in the postoperative period, lessening the risk of
pelvic sepsis.
Aer the patient recovers fully, regains optimal nutritional status,
and is no longer taking high-dose immunosuppressive medication,
the subtotal colectomy with ileostomy can be followed by an elective
reconstructive procedure. In patients with IBD, the type—UC, Crohn
disease, or indeterminate colitis—determines the recommended subsequent surgery. Patients with UC may elect a completion proctocolectomy with an ileoanal pouch, a permanent end ileostomy, or a
continent ileostomy (Kock pouch). Depending on the status of the
rectum, patients with Crohn disease may consider an ileorectal anastomosis or retain the end ileostomy because an ileoanal pouch is generally contraindicated.
A total proctocolectomy is infrequently performed in the setting of toxic colitis and is not advised for toxic megacolon because
an emergency total proctocolectomy carries a higher mortality and
morbidity rate than subtotal colectomy. e procedure risks complications such as small bowel obstruction, hemorrhage, pelvic nerve
damage, stula, and pelvic sepsis as a result of the rectal dissection,
particularly of an acutely inamed rectum. Possible indications for
the procedure are colonic hemorrhage, including from the rectum;
a rectal perforation; or a patient who prefers a permanent ileostomy
without any eventuality of an ileoanal pouch. If a total proctocolectomy is undertaken, the anal sphincters should be le intact to preserve the option of a subsequent ileoanal pouch procedure. However,
despite the preoperative diagnosis, the patient may ultimately be
determined to be ineligible for a pelvic pouch, whether because of
comorbidities or a later diagnosis of Crohn disease (the diagnosed
IBD variant changes in approximately 40% of patients based on the
colectomy specimen). Most commonly, an ileal pouch–anal anastomosis is completed electively aer a subtotal colectomy with ileostomy, using either the two- or three-stage technique. Immediate
pouch construction is not recommended.
The Turnbull procedure was developed in the 1970s as a
technique for dealing with the extremely fragile colon that was
then seen in patients with toxic megacolon. It involved creating
a loop ileostomy and a colonic “blowhole”—a cutaneous colostomy—to decompress the diseased colon. The loop ileostomy is
irst created in the right lower quadrant via a small lower midline
f
incision. Once this incision is closed, a 4- to 6-cm vertical midline or paramedian incision is made directly over the previously
marked location of the dilated transverse colon; the transverse
colon is then decompressed via a 14-gauge needle and a colostomy is fashioned at the skin level. By this minimal dissection of
the fragile, distended colon, iatrogenic perforation is prevented. A
free perforation, colonic hemorrhage, and generalized peritonitis
are contraindications for the procedure. After 4 to 6 months, the
procedure is then followed by an elective colectomy or, in rare
cases, closure of the stoma. This operation is rarely performed
now because the extreme fragility of the bowel seen in Turnbull’s
day is no longer a feature of the disease. However, the procedure
may be advantageous for extremely poor surgical candidates or for
patients with multiple contained colonic perforations, as well as
for pregnant patients with toxic colitis.
CONCLUSION
dvances in medical management and surgical techniques over the
A
decades have improved outcomes in patients with toxic colitis and
megacolon. Corticosteroids, newer second-line agents, and enhanced
critical care support have further beneted these sick patients, allowing many to avoid a colectomy. However, a signicant proportion
of these patients still require surgery at the time of admission, and
better results are obtained with an early intervention. e addition
of the new “rescue” medications has the potential to delay surgery,
sometimes to the detriment of the patient. e role for the secondline rescue agents and their impact on the timing of surgery should
be further elucidated. Toxic colitis and megacolon are still aliated
with signicant morbidity and mortality. e successful management of these patients relies upon the input of both surgeons and
gastroenterologists.
S
g g e
u
Au
sch C, Mado RD, Gnant M, etal. Aetiology and surgical management of
toxic megacolon. Colorectal Dis. 2005;8:195–201.
Fazio VW. Toxic megacolon in ulcerative colitis and Crohn’s colitis. Clin
Gastroenterol. 1980;9:389–407.
Holubar SD, Larson DW, Dozois EJ, etal. Minimally invasive subtotal colec-
tomy and ileal pouch-anal anastomosis for fulminant ulcerative colitis: a
reasonable approach? Dis Colon Rectum. 2009;52:187–192.
Ross H, Steele SR, Varma M, etal. Practice parameters for the surgical treatment
of ulcerative colitis. Dis Colon Rectum. 2014;57:5–22.
Teeuwen PHE, Stommel MWJ, Bremers AJA, etal. Colectomy in patients with
acute colitis: a systematic review. J Gastrointest Surg. 2009;13:676–686.
Windsor A, Michetti P, Bemelman W, Ghosh S. e positioning of colectomy
in the treatment of ulcerative colitis in the era of biologic therapy. Inamm
Bowel Dis. 2013;19:2695–2703.
e d Rea d i n g
S t
P:
P
C
T M
INTR
ODUCTION
W
hen a total proctocolectomy is required, the ileal pouch–anal anastomosis (IPAA) procedure is favored over an end ileostomy because
the IPAA allows continence with defecation by the normal route.
e procedure can be performed with favorable results for patients
with ulcerative colitis and familial adenomatous polyposis, as well
as in some patients with indeterminate colitis and highly selectively
in patients with Crohn disease that is conned to the large intestine. Good early and long-term function and quality of life can be
expected; however, because complications inuence long-term
results and hence pouch retention, sound surgical decision making
and use of sound technique are critical.
Use of strategies that can target modiable risk factors for complications and reduce risk in persons most likely to have complications optimizes good long-term outcomes. A staged procedure with
an initial subtotal colectomy reduces risk of complications in highrisk patients with poor general health or malnutrition, in patients
receiving high doses of immunosuppressive drugs or who are being
treated with steroids, and in patients who have severe acute colitis.
Similarly, an awareness of the perioperative complications that can
occur facilitates their identication and prompt management, which
aects both short-term results and long-term pouch function and
retention.
For certain pouch-related problems, correction by both perineal
and abdominal approaches is feasible, allowing the pouch to be salvaged. Pouch failure is generally dened as the need for the creation
of a permanent ostomy with or without excision of the pouch. Factors
shown to be associated with pouch failure include certain diseases
(e.g., Crohn disease), prior anal disease, abnormal anal manometry
ndings, comorbid conditions, pouch-perineal or pouch-vaginal
stulae, pelvic sepsis, and anastomotic stricture and separation. e
following preoperative factors have the strongest inuence on pouch
survival: extent of resection (total proctocolectomy vs. completion
proctectomy), type of anastomosis (stapled vs. hand sewn), patient
diagnosis (mucosal ulcerative colitis and others vs. Crohn disease),
and comorbidity. In this chapter, various complications related to the
ileoanal pouch—several of which may lead to pouch failure—and
their management are discussed.
Ra
vi P. Kiran
mptoms need to be obtained. e state of the anoperineum and
sy
the integrity of the sphincter mechanism are assessed by examination, followed by pouchoscopy with biopsies of the pouch, residual
anal canal, and aerent limb. Biopsies help evaluate the presence of
inammation, suggesting pouchitis or cutis, Crohn disease, or other
inammatory and infectious complications. Stool and blood tests
help exclude an infection as the cause of the changes in pouch function. e potential diagnosis of Crohn disease needs to be considered
in any patient who experiences stulous and septic complications
aer creation of an ileoanal pouch. However, septic complications
aer ileoanal pouch creation may mimic Crohn disease, and the
distinction may be challenging. In general, septic complications that
occur within 1 year of pouch creation or closure of a defunctioning
ostomy above a pouch are likely to be due to perioperative anastomotic or pelvic infections. If complications occur more than 1 year
aer creation of the pouch, the degree of suspicion for Crohn disease
should increase.
A Gastrogran enema helps evaluate pouch structure and capacity and identify pouch-perineal or pouch-vaginal stulae, narrowing
of the aerent limb, inlet, or outlet, and any posterior sinus tract leading from the anastomosis. Magnetic resonance imaging (MRI) of the
pelvis helps detect any persistent presacral collections, abscesses, or
stulae that could be contributing to the patient’s symptoms. Computed tomography (CT) enterography is useful in the evaluation of
the small intestine proximal to the pouch; inammation indicates
the possibility of Crohn disease. Anorectal manometry and endoanal
ultrasound are used to assess the sphincter tone, anatomic integrity,
and presence of paradoxical pressures, which, when correlated with
diculties with evacuation, suggest outlet obstruction. A defecating
pouchogram or magnetic resonance defecography identies problems with evacuation.
INTRA
ntraoperative complications specically related to pouch creation
I
include bleeding, diculty with reach of the pouch, and pouch ischemia resulting either from tension or extrazealous attempts at vascular division to allow an ileoanal pouch to reach to the residual anal
canal.
OPERATIVE COMPLICATIONS
POUCH D
atients with a well-constructed, uncomplicated ileoanal pouch typi-
P
cally have six to eight bowel movements over a 24-hour period. Most
patients do not need to wear pads, although some patients do so for
peace of mind. Patients can defer defecation for at least an hour, and
incontinence is rare. Quality of life is high, and most patients deny
having physical, social, work-related, or sexual restrictions.
When patients experience pouch dysfunction, a detailed history
of symptoms, function of the pouch, and the timing of the onset of
YSFUNCTION
POST
ostoperative complications include pelvic sepsis, anastomotic dehis-
P
cence, pouch bleeding, pouch-perineal and pouch-vaginal stulae,
pouch sinus, leak from the tip of the J limb, pouch prolapse, pouchitis and cutis, Crohn disease of the pouch, outlet dysfunction,
pouch cancer, and pouch failure. Late complications typically occur 3
months aer creation of the pouch or aer takedown of the ileostomy
when the pouch has been defunctioned.
OPERATIVE COMPLICATIONS
197
198
Pel
vic Pouch:
comPlic
ations and
their mana
gement
Pelvis Sepsis and Anastomotic Leak
Ile
oanal pouch–related pelvic sepsis is a complication of varying
degrees of severity, and apart from leading to poor outcomes over the
short and intermediate term, it may predispose to pouch failure. Even
when the sepsis is successfully treated, patients may have impaired
long-term function and a reduced quality of life. A careful assessment of potentially predisposing factors, together with preoperative
and intraoperative planning to minimize their aect, is important.
A high body mass index, a nal pathologic diagnosis of ulcerative/
indeterminate colitis or Crohn disease, and use of intraoperative and
postoperative transfusions are associated with pelvic sepsis.
Pelvic sepsis may occur as a result of, or separate from, an anastomotic dehiscence. Pelvic sepsis presents with fever, leukocytosis,
tachycardia, and pelvic or lower back pain, although the symptoms
can be nonspecic, such as an ileus or a delayed recovery. A CT scan
of the abdomen and pelvis with use of oral, intravenous, and rectal
contrast material is useful in identifying a peripouch abscess and its
communication with any anastomotic leak. Unstable patients require
an emergency exploratory laparotomy with peritoneal washout and
an ostomy if the pouch has not already been defunctioned. In some
cases, a loop ileostomy above a pouch may need to be converted to
an end ostomy. In stable patients, percutaneous or transanal drainage of the abscess in conjunction with administration of antibiotics
is required for prompt control of sepsis, which may allow preservation of the pouch. For abscesses communicating with the anastomosis, drainage can be transanal or percutaneous, and if percutaneous,
drainage can occur by transabdominal or transgluteal routes.
Postoperative Bleeding from the Pouch
e long suture or staple line within the pouch predisposes patients
to perioperative bleeding, which usually presents as anal bleeding or
blood from the ostomy. Although severe bleeding is uncommon, it
may be troublesome. Oversewing of the back row of staples along
the mesentery of the small bowel aer the pouch is created may
minimize the chances of postoperative bleeding. Pouchoscopy with
cautery, application of hemostatic clips, or injection of epinephrine
usually controls bleeding. When diuse oozing occurs, a continuous
irrigation of the pouch with saline solution/epinephrine through the
downstream end of the ileostomy with recovery of the uid through
a catheter placed in the anus usually facilitates control.
which allows the most thorough evaluation of the pouch and
perineum and provides the best information. Other tests that
should be considered include a Gastrogran enema, vaginography,
and MRI of the pelvis because these tests help dene the presence
and anatomy of a stula. CT or magnetic resonance enterography
show both the anatomy of the pouch and the state of the small
bowel above the pouch.
When active sepsis is present, the rst priority is to obtain control
by adequate drainage of any abscess cavity or infected track, which
helps resolve symptoms and limits further tissue damage. If local
drainage is unsuccessful in controlling the sepsis, then antibiotics,
antiinammatory agents, or specic Crohn disease medications may
help. e nal step in controlling the sepsis is fecal diversion. Once
the sepsis is controlled and has settled, options for repair of the stula
can be entertained.
Local procedures may be considered for low, simple, pouchrelated fistulae and include pouch or vaginal advancement flap
repairs, perineal pouch advancement, fistula glue or plugs, and
gracilis flap repair or interposition of a biologic mesh. If the
perineal, local, or pouch advancement repair fails, subsequent
attempts at local flap repair may be made. When perineal pouch
advancement is undertaken, half of the pouch–anal anastomosis
adjoining the location of the fistula is disconnected and the entire
pouch wall is mobilized transanally prior to approximation to the
anal canal with or without mucosectomy. A repeat IPAA is also
an option for patients in whom repair by the perineal approach is
unlikely to be successful and when local procedures have definitively failed. Crohn disease must first be excluded to the extent
possible. The pouch is disconnected from the anus by combined
abdominoperineal dissection and is then revised with excision
and debridement of the portion involved in the fistula tract. Any
defect in the rectovaginal septum is repaired, and a mucosectomy
and a hand-sewn anastomosis is performed. The previous pouch
may be reused, refashioned, or augmented as needed, or a new
pouch may be created after resection of the previous pouch. An
omental pedicle flap can be used to separate the pouch from the
vagina.
Up to 85% of pouch-vaginal stulae can be healed using these
approaches, resulting in a pouch failure rate of 15%. For the 15% of
persons who experience pouch failure, pouch excision with an end
ileostomy or conversion of the J pouch to a K pouch is performed.
ouch Sinus
P
Pouch-Perineal and Pouch-Vaginal Fistulae
A
stula from the pouch or the pouch anal anastomosis to the vagina
or the perineal skin presents with increasing pain and local sepsis
that ultimately leads to discharge of pus or stool and gas. A stula
may occur aer drainage of a pouch or an anastomotic leak. e
patient also may experience discomfort, irritation, and incontinence,
as well as recurrent vaginal and urinary infections. Fistulas may present soon aer ileostomy closure or construction of an undiverted
pouch or some months later. A thorough review of the history and
medical records relating to the ileoanal pouch surgery, the postoperative course aer the procedure, and a pathology review of biopsies
from prior to surgery, as well as of the colectomy or proctocolectomy
specimen, may help achieve a better assessment of the pathologic
diagnosis and particularly establish the possibility of Crohn disease.
General, abdominal, and perineal examination for clinical indications of Crohn disease, together with the function of the anal sphincter, provides useful information.
Vaginoscopy and pouchoscopy may allow for both the identication of the stula and a determination of the location, number,
nature, and size of the stulous openings, together with an assessment of the physical state of the pouch, anal canal, and vagina.
is examination is best performed aer induction of anesthesia,
A
pouch sinus is a blind track that comes from an opening at the
anastomosis or in the pouch itself. is complication occurs in
2.8% to 8% of patients aer an IPAA procedure. e sinus track
may be of variable size, its opening may be narrow or wide-necked,
and it may be either incidental or symptomatic. When symptoms
occur, they may either be minor or major, such as sepsis, pelvic
pain, pouch dysfunction, and even pouch failure. Presentation
with symptoms is a signicant predictor for low healing rates and
pouch failure.
erapeutic options include debridement, unroong, use of
brin glue, pouch revision, and creation of a new pouch. e choice
of treatments depends on the presentation, size, location, and other
factors, such as whether the pouch is defunctioned. In asymptomatic patients and in patients with a proximal ostomy in whom the
condition is detected incidentally, spontaneous healing occurs with
ime. For a symptomatic sinus, transanal drain placement, deroong,
t
or sinusotomy may be an option, with the creation of an ostomy to
cover a pouch that is not defunctioned. For an incidental sinus in a
patient with a diverted pouch, the sinus may be opened or repaired
prior to closure. Sometimes closure can proceed with no treatment if
the sinus appears harmless. When healing does not occur in symptomatic patients, a repeat IPAA or pouch excision with an ileostomy
may be considered.
Leak fr
L
at the ileal anal pouch anastomosis are rare. A leak from the tip of
the J pouch is uncommon and dicult to detect because the hole in
the pouch is not in the direct ow of the fecal stream; thus symptoms are subtle and the presentation is indolent. Patients present
with nonspecic and usually subacute symptoms such as abdominal pain, fever, or diarrhea. In some patients, leaks may present
with a stula rather than a pelvic abscess, a presentation usually
suggestive of an anastomotic leak or Crohn disease. Pouchoscopy,
a Gastrogran enema, a CT scan with use of a rectal contrast
agent, or an MRI scan of the pelvis may detect the site of the leak,
although sometimes detection may only be possible upon laparotomy. A high degree of suspicion is required for its diagnosis, and
when detected, management depends upon the nature and degree
of the defect and associated ndings in the pouch and pelvis. Salvage surgery may require pouch repair of the leak site, a pouch
revision, or pouch resection with a repeat IPAA with or without a
proximal ostomy.
P
P
occurs in 0.3% of patients in whom a pouch is created. Patients may
present with tissue prolapse or outlet dysfunction, and clinical examination, manometry, and pouchoscopy may suggest the diagnosis. In
patients with mucosal prolapse, stool bulking agents and biofeedback
are initially utilized in an attempt to avoid excessive straining. When
symptoms persist, a local perineal procedure with pouch advancement aer the excision of redundant mucosal tissue can be considered. For patients with full-thickness pouch prolapse, denitive
transabdominal surgery may be the best treatment. Pouchpexy using
a transabdominal approach, with xation of pouch to the sacrum
with nonabsorbable sutures, is a reasonable option.
P
P
ing of the residual anal canal and are diagnosed at pouchoscopy and
biopsy. Treatment is primarily medical. Small areas of cu inammation may be approached through ablative or excisional means.
However, a defunctioning ostomy or pouch excision with an end
ileostomy may be required for recalcitrant pouchitis or cutis that
is unresponsive to medical treatment. Corrective surgery or a repeat
IPAA also may be required for the management of pouchitis resulting
from complications of the pouch such as a chronic presacral abscess,
a pouch sinus, small pouch size, or obstruction resulting from a stricture or pouch prolapse. A repeat IPAA is also an option for proctitis
resulting from a long rectal remnant retained at the time of IPAA.
Recurrent cutis occasionally can be managed with a mucosectomy
and perineal pouch advancement.
om the Tip of the “J”
eaks from suture and staple lines in the pouch that are not located
ouch Prolapse
ouch prolapse is a rare complication of the ileoanal pouch that
ouchitis and Cuffitis
ouchitis and cutis relate to inammation of the pouch or the lin-
COLON
o-side anastomosis between the strictured segment and the
side-t
top of the pouch. Strictures of the pouch body similarly can be
managed with a stricturoplasty. Such treatment is usually combined with a defunctioning ostomy above the pouch and medical
treatment of the Crohn disease. More extensive disease involving
the pouch may lead to pouch excision or permanent defunction.
Surgical management of strictures of the pouch–anal anastomosis may include dilatation, stricturoplasty, diversion, or a repeat
IPAA. Perianal disease may be managed with drain or seton placement to allow drainage of loculated abscesses or fistulae in combination with medical treatment.
199
Outlet Dysfunction
roblems with pouch evacuation may develop as a result of a stricture
P
at the anastomosis or pouch prolapse. Strictures resulting from scar
tissue or Crohn disease can be managed by periodic self-dilatation,
endoscopic balloon dilatation, serial bougie dilatation, or a stricturoplasty. For outlet dysfunction that occurs in the absence of an
anatomic cause, evaluation of the pelvic oor may reveal paradoxical
contraction of the puborectalis. Biofeedback is an option for these
patients, and injection of the pelvic oor with botulinum toxin A
(Botox) can be attempted. Enemas and intermittent self-intubation
of the pouch with irrigation may be useful in both organic and functional obstructive disorders.
In patients with an S pouch, a long spout may cause problems
with defecation. e spout should be no longer than 2 cm. Transanal
shortening of the spout may help.
Cancer of the P
ancer of the pouch itself is rare, even in patients with familial ade-
C
nomatous polyposis. Cancer in the anal transition zone arising from
residual rectal mucosa is more common, although still rare. Mucosectomy with a hand-sewn anastomosis does not eliminate the risk of
cancer, but the risk is less than that of a stapled IPAA. A stapled ileal
pouch anal anastomosis may facilitate surveillance of the pouch and
anal transitional zone, but patients are at risk for cancer aer both
types of anastomoses.
ouch Failure
P
hen pouch failure develops, surgical options include pouch
W
excision with a temporary or permanent end ileostomy, pouch
revision or creation of a new pouch, conversion of the J pouch
to a K pouch, and the creation of an ostomy above a pouch left in
situ. In the latter instance, provided symptoms from the retained
pouch are not unmanageable and do not impinge on quality of life,
the pouch can be retained for an extended period. In these circumstances, periodic surveillance of the pouch with surveillance
biopsies is necessary.
ouch
Cr
ohn Disease of the Pouch
ohn disease may affect the body of the pouch, the afferent
Cr
limb, the pouch-anal anastomosis, the perineum, or the small
intestine proximal to the pouch. Medical management includes
steroids, immunosuppressive medication, and/or biologic agents.
Endoscopic intervention, including dilatation, may be used for
isolated short-segment strictures of the pouch-anal anastomosis,
pouch body, or afferent limb. Surgical treatment may be required
for strictures that are not amenable to endoscopic therapy and
when endoscopic therapy fails. Strictures of the afferent limb
may require small bowel resection or stricturoplasty or rarely a
ABDOMINOPERINEAL APPR
OACH FOR
POUCH SALVAGE
Repeat abdominal surgery with abdominoperineal reconstruction or
revision of the ileal pouch with or without the creation of a neoileal
pouch-anal anastomosis is a reasonable option for select patients
with a failed pouch. Pouch salvage is associated with acceptable
functional outcomes and quality of life. When matched with patients
who underwent primary IPAA, patients who underwent creation of a
new pouch reported greater seepage during the day and at night and
greater daytime pad usage aer a median follow-up of 5 years, but
other functional outcomes and quality of life are similar.
200
Operativ
W
ith the patient in the Lloyd-Davies position, the abdomen and
Pel
vic Pouch:
e Technique
comPlic
ations and
their mana
perineum are prepared and draped. e placement of bilateral ureteral stents allows the identication of the ureters and detection
of any injury. e abdomen is entered through the previous incision, and the small bowel mesentery and pouch are mobilized to
the pelvic oor, ensuring preservation of the presacral nerves and
other pelvic structures. e pouch is then disconnected from the
anastomosis, delivered into the abdomen, and evaluated. e state
and residual capacity of the pouch, the length of remaining small
intestine, and the potential problems with reach of the pouch to
the anal canal are then evaluated. e old pouch is either revised
or excised, with a new pouch created prior to reanastomosis. If the
repeat IPAA is performed because of pouch failure resulting from
a chronic presacral abscess cavity, the abscess is drained and the
cavity walls are debrided. A repeat IPAA is performed in a handsewn manner aer a mucosectomy to the level of the dentate line
is performed. A diverting loop ileostomy is usually created, or the
existing ileostomy is le is in place. When the pouch is healthy or
can be repaired but a repeat anastomosis is not feasible because
of problems with reach, scarring in the pelvis, or poor sphincter
tone, or if a repeat pouch procedure is not chosen by the patient,
the pouch can be retained as a continent ileostomy. In this case,
the pouch is the reservoir and a length of the small bowel proximal
to the pouch is divided and used to create the nipple valve and
exit conduit, aer which the proximal cut end of the small bowel
is anastomosed to the pouch aer pouch rotation. When pouch
gement
cision with a permanent end ileostomy is performed, manage-
ex
ment of the anal canal remnant is determined by reasons for pouch
failure, the state of the perineum and sphincter mechanism, and
the presence or absence of associated sepsis.
g g e
u
S
A
Fazio VW, Tekkis PP, Remzi F, etal. Quantication of risk for pouch failure
Johnson PM, O’Connor BI, Cohen Z, McLeod RS. Pouch-vaginal stula aer
Kiran RP, da Luz Moreira A, Remzi FH, et al. Factors associated with
Manilich E, Remzi FH, Fazio VW, etal. Prognostic modeling of preoperative
Nyam DC, Wol BG, Dozois RR, etal. Does the presence of a pre-ileostomy
Remzi FH, Fazio VW, Kirat HT, etal. Repeat pouch surgery by the abdomi-
Shah NS, Remzi F, Massmann A, etal. Management and treatment outcome
S t
kbari RP, Mado RD, Parker SC, etal. Anastomotic sinuses aer ileoanal
pouch construction: incidence, management, and outcome. Dis Colon
Rectum. 2009;52:452–455.
aer ileal pouch anal anastomosis surgery. Ann Surg. 2003;238(4):605–
614. discussion 614–617.
ileal pouch-anal anastomosis: treatment and outcomes. Dis Colon Rectum.
2005;48(6):1249–1253.
septic complications aer restorative proctocolectomy. Ann Surg.
2010;251(3):436–440.
risk factors of pouch failure. Dis Colon Rectum. 2012;55(4):393–399.
closure asymptomatic pouch-anastomotic sinus tract aect the success of
ileal pouch-anal anastomosis? J Gastrointest Surg. 1997;1:274–277.
nal approach safely salvages failed ileal pelvic pouch. Dis Colon Rectum.
2009;52(2):198–204.
of pouch-vaginal stulas following restorative proctocolectomy. Dis Colon
Rectum. 2003;46:911–917.
e d
R
e
a d i n g